May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Blockade of RAGE supresses hypoxia–induced Egr–1 expression in the retina
Author Affiliations & Notes
  • S.R. Tari
    Ophthalmology,
    Columbia University, New York, NY
  • S.E. Lee
    Ophthalmology,
    Columbia University, New York, NY
  • J.J. Tseng
    Ophthalmology,
    Columbia University, New York, NY
  • D. Onat
    Medicine,
    Columbia University, New York, NY
  • S.I. Pachydaki
    Internal Medicine, The Cleveland Clinic Foundation, Cleveland, OH
  • H. Hörig
    Surgery,
    Columbia University, New York, NY
  • D.N. Moroziewicz
    Surgery,
    Columbia University, New York, NY
  • S.F. Yan
    Surgery,
    Columbia University, New York, NY
  • A.M. Schmidt
    Surgery,
    Columbia University, New York, NY
  • G.R. Barile
    Ophthalmology,
    Columbia University, New York, NY
  • Footnotes
    Commercial Relationships  S.R. Tari, None; S.E. Lee, None; J.J. Tseng, None; D. Onat, None; S.I. Pachydaki, None; H. Hörig, None; D.N. Moroziewicz, None; S.F. Yan, None; A.M. Schmidt, None; G.R. Barile, None.
  • Footnotes
    Support  support: Research to Prevent Blindness
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 1187. doi:
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      S.R. Tari, S.E. Lee, J.J. Tseng, D. Onat, S.I. Pachydaki, H. Hörig, D.N. Moroziewicz, S.F. Yan, A.M. Schmidt, G.R. Barile; Blockade of RAGE supresses hypoxia–induced Egr–1 expression in the retina . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1187.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Previous studies have suggested key roles for egr–1 in upregulation of inflammatory and prothrombotic genes in the cardiovascular system in hypoxia. Uprgulation of Egr–1 may lead to cellular dysfunction such as increased vascular permeability and induction of apoptosis cascades. This study sought to examine the effects of blockade of the proinflammatory receptor for advanced glycation end product (RAGE) axis upon hypoxia–induced Egr–1 expression in the retina. Methods: Twelve C57/blk6 mice were divided into four groups: 1) Untreated controls; 2) Treated controls administered two intraperitoneal doses of sRAGE (soluble receptor for advanced glycation end products, a competitive inhibitor for RAGE, injected 24 hours and 30 minutes prior to sacrifice); 3) Hypoxic mice placed in a chamber for 6 hours at 6–6.5% O2 concentration; and 4) Treated, hypoxic mice administered two doses of sRAGE as in the second group and placed in the hypoxia chamber simultaneously with the third group. Animals were immediately sacrificed, the eyes enucleated, and the retinas isolated and prepared for quantitative PCR analysis. One eye of each group was put in 4% paraformaldahyde for use in immunohistochemistry. Results: Quantitative gene analysis by real–time PCR showed a 4.3 fold elevation of Egr–1 mRNA levels, and this elevation was reversed by blockade of RAGE using sRAGE. Immunostaining for Egr–1 suggested zones of co–localization with RAGE in the inner retina.  

Conclusion: These findings suggest key roles for the RAGE–dependent mechanisms in regulation of egr–1 in hypoxic stress in the retina.

Keywords: hypoxia • retinal neovascularization • gene/expression 
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